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It is difficult to link exposures to specific carcinogens with the development of cancer, since latency is generally quite long and the nature of exposure is poorly documented Environmental carcinogens include chemical carcinogens such as benzene and asbestos, oncogenic viruses such as the human papillomavirus and the Epstein Barr virus, and physical agents such as ionizing radiation and ultraviolet light Certain viral infections may increase the risk of cancer and clearly have a pathogenetic role, such as the association between Epstein Barr virus infection and endemic Burkitt s lymphoma and non-Hodgkin s lymphoma Chronic infection with hepatitis B or C viruses increases the risk of hepatocellular carcinoma Infection with HIV has been associated with non-Hodgkin s lymphoma, Hodgkin s disease, Kaposi s sarcoma (KS), and cervical and anal cancers The finding of human herpesvirus-8 (HHV-8) DNA sequences in both AIDS-associated and non AIDS-associated KS supports a causative role of the herpesviruses in the development of some cancers It appears that HHV-8 is sexually transmitted among men Antibodies to HHV-8 correlate with the subsequent development of KS and it is now thought that infection is necessary for KS to develop The sexually transmitted human papillomavirus (HPV) is a major risk factor for the development of cervical carcinoma and anal cancer; nearly 100% of women with cervical cancer have evidence of this infection Fifteen HPV subtypes have been identified with an increased risk of cervical cancer; HPV 16 and 18 are the most common and are associated with a more than 200-fold increased risk of cancer HPV is a common infection, and most infected women do not develop cancer Progression is associated with persistent infection over a decade or more; additional genetic or systemic cofactors are required, although only partially understood Understanding the infectious cause of cervical cancer has led to the development of highly effective vaccines that appear to prevent infection and the development of precancerous lesions One vaccine is now FDA approved to prevent this sexually transmitted oncogenic infection Chronic infection with bacteria has also been associated with an increased risk of malignancy Infection with Helicobacter pylori is thought to increase the risk of cancer of the distal portion of the stomach approximately sixfold and also increases the risk for gastric lymphoma Approximately 60% of gastric cancers are associated with H pylori infection Geographic variations in the incidence of gastric cancer appear to be influenced by geographic variations in the strain of H pylori; strains that produce a specific protein are more likely to be associated with cancer than those that do not Screening for and treatment of H pylori may be a cost-effective way to prevent gastric cancer in the United States An additional cause of cancer is chemotherapy or radiation therapy for a prior malignancy More aggressive chemothera-.

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peutic and radiation regimens and especially those combining the two treatment modalities have been associated with increased rates of both secondary leukemias and solid tumors The latency period may be short (2 5 years for leukemia) or very long (10 20 years for solid tumors), but the prognosis is uniformly poor Chemotherapeutic agents known to cause secondary malignancies include alkylating agents busulfan, cyclophosphamide, mechlorethamine, etc and topoisomerase II inhibitors, including epipodophyllotoxins (etoposide), anthracyclines, ie, doxorubicin and epirubicin, and anthracenediones (mitoxantrone) Secondary leukemias can be characterized to some degree by the causative agent Alkylator-induced leukemias are usually associated with abnormalities involving chromosomes 5 and 7 and generally occur within 5 7 years after exposure In contrast, topoisomerase II-induced leukemias occur within 2 3 years following exposure and involve aberrations in a specific gene within the long arm of chromosome 11 (11q23) Abnormalities of 11q23 often occur at a specific breakpoint region thought to be involved in DNA transcription An increase in the rate of secondary acute leukemia has been reported in breast cancer patients treated with dose intensification of cyclophosphamide in combination with doxorubicin (a topoisomerase II active drug) from 1992 to 1994 The incidence is approximately 03% in a multicenter study involving over 2500 women with positive axillary nodes Increased dosages and frequency of administration of anthracyclines, anthracenediones, and the alkylating agent cyclophosphamide have been reported to increase the risk of leukemia to as high as 3 4% Prolonged oral exposure to etoposide or alkylator agents can result in a much higher risk of secondary leukemia as well Platinum-based chemotherapy for ovarian cancer has been reported to increase the risk of leukemia twofold to eightfold, with larger doses and longer treatment courses associated with higher risks This risk was significantly higher in women who had also received intravenous melphalan The risk of certain secondary cancers may be age dependent Radiation therapy for Hodgkin s disease increases the risk of breast cancer (including bilateral disease), particularly if the radiation occurred in women under the age of 30 years The relative risk of subsequent solid tumors and leukemias has been found to increase significantly with younger age at first chemotherapy treatment for Hodgkin s disease This risk is especially high when chemotherapy and radiation are combined Nevertheless, the risk of secondary malignancies in children surviving at least 5 years after diagnosis is relatively low at 32% 20 years postdiagnosis, with primary disease recurrence remaining the most common cause of mortality The Childhood Cancer Survivor Study (CCSS) is a large prospective study of over 14,000 survivors of childhood cancer designed to characterize the late effects of therapy in this increasing population Although the risk of complications is highest in the first 5 years after diagnosis and treatment, risks of additional sequelae persist for many years.

Edwards BK et al Annual report to the nation on the status of cancer, 1975-2002, featuring population-based trends in cancer treatment J Natl Cancer Inst 2005 Oct 5;97(19):1407 27 [PMID: 16204691]

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